Interferon-γ inhibits group B Streptococcus survival within human endothelial cells

Abstract

Endothelial dysfunction is a major component of the pathophysiology of septicaemic group B Streptococcus (GBS) infections. Although cytokines have been shown to activate human umbilical vein endothelial cells (HUVECs), the capacity of interferon (IFN)-γ to enhance the microbicidal activity of HUVECs against GBS has not been studied. We report that the viability of intracellular bacteria was reduced in HUVECs activated by IFN-γ. Enhanced fusion of lysosomes with bacteria-containing vacuoles was observed by acid phosphatase and the colocalisation of Rab-5, Rab-7 and lysosomal-associated membrane protein-1 with GBS in IFN-γ-activated HUVECs. IFN-γ resulted in an enhancement of the phagosome maturation process in HUVECs, improving the capacity to control the intracellular survival of GBS.

Group BStreptococcusInduces a Robust IFN-γResponse by CD4+T Cells in anIn VitroandIn VivoModel

“…While IL-10, IL-12, and IL-18 are beneficial [ 6 – 9 ], TNF- α contributes to GBS-induced sepsis [ 7 , 10 ]. IFN- γ appears promising for control of GBS disease; IL-12 and IL-18 exert therapeutic effects by stimulating immune cells to produce IFN- γ [ 6 , 8 , 9 ], IFN- γ production is impaired in neonates and this might partly explain their susceptibility to GBS infection [ 8 , 11 , 12 ], and IFN- γ inhibits GBS survival in human endothelial cells [ 13 ]. Although NK and NKT cells have been proposed to secrete IFN- γ in response to GBS [ 14 , 15 ], no specific cell line has been clearly identified yet as a major source.…”